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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2010-6-14
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pubmed:abstractText |
Virulence of emerging community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) and other highly pathogenic S. aureus strains depends on their production of phenol-soluble modulin (PSM) peptide toxins, which combine the capacities to attract and lyse neutrophils. The molecular basis of PSM-stimulated neutrophil recruitment has remained unclear. Here, we demonstrate that the human formyl peptide receptor 2 (FPR2/ALX), which has previously been implicated in control of endogenous inflammatory processes, senses PSMs at nanomolar concentrations and initiates proinflammatory neutrophil responses to CA-MRSA. Specific blocking of FPR2/ALX or deletion of PSM genes in CA-MRSA severely diminished neutrophil detection of CA-MRSA. Furthermore, a specific inhibitor of FPR2/ALX and of its functional mouse counterpart blocked PSM-mediated leukocyte infiltration in vivo in a mouse model. Thus, the innate immune system uses a distinct FPR2/ALX-dependent mechanism to specifically sense bacterial peptide toxins and detect highly virulent bacterial pathogens. FPR2/ALX represents an attractive target for new anti-infective or anti-inflammatory strategies.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1934-6069
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pubmed:author |
pubmed-author:BohnErwinE,
pubmed-author:BoulayFrancoisF,
pubmed-author:GleskeAnne-KathrinAK,
pubmed-author:KöberleMartinM,
pubmed-author:KlebanoffSeymour JSJ,
pubmed-author:KretschmerDorotheeD,
pubmed-author:OttoMichaelM,
pubmed-author:PeschelAndreasA,
pubmed-author:RabietMarie-JosépheMJ,
pubmed-author:RautenbergMarenM,
pubmed-author:SchönebergTorstenT,
pubmed-author:WangRongR,
pubmed-author:van KesselKok AKA,
pubmed-author:van StrijpJos AJA
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pubmed:copyrightInfo |
Copyright (c) 2010 Elsevier Inc. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:day |
25
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pubmed:volume |
7
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
463-73
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pubmed:meshHeading |
pubmed-meshheading:20542250-Animals,
pubmed-meshheading:20542250-Bacterial Toxins,
pubmed-meshheading:20542250-Community-Acquired Infections,
pubmed-meshheading:20542250-Female,
pubmed-meshheading:20542250-Host-Pathogen Interactions,
pubmed-meshheading:20542250-Humans,
pubmed-meshheading:20542250-Methicillin-Resistant Staphylococcus aureus,
pubmed-meshheading:20542250-Mice,
pubmed-meshheading:20542250-Mice, Inbred BALB C,
pubmed-meshheading:20542250-Models, Biological,
pubmed-meshheading:20542250-Neutrophils,
pubmed-meshheading:20542250-Protein Binding,
pubmed-meshheading:20542250-Receptors, Formyl Peptide,
pubmed-meshheading:20542250-Receptors, Lipoxin,
pubmed-meshheading:20542250-Staphylococcal Infections
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pubmed:year |
2010
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pubmed:articleTitle |
Human formyl peptide receptor 2 senses highly pathogenic Staphylococcus aureus.
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pubmed:affiliation |
Cellular and Molecular Microbiology Division, Interfaculty Institute of Microbiology and Infection Medicine, University of Tübingen, Elfriede-Aulhorn-Strasse 6, 72076 Tübingen, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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